It is estimated that over 1.5 million cases of poison ivy are encountered every year with a concomittant loss of over 152,000 work days in the United States. There are no successful treatments known in the art for developing tolerance in, or desensitization of sensitive mammals to poison ivy or the related allergenic causing plants of the Anacardiaceae family.
The methods employed to attempt treatment or prevention of dermatitis caused particularly by contact with poison ivy, poison oak and poison sumac have, historically, followed three avenues of approach namely, antigens, topical agents, and chemical barriers. For brevity in this discussion, the term allergenic agent is to be understood to include the allergenic agents contained in poison ivy, poison oak, poison sumac and cashew nut shell oil, which are the principal dermatitis causing plants and substances of the family Anacardiaceae found all over the world. Of these plants, poison ivy, per se, is the most widely distributed species in the United States. There are many species of poison ivy in North America. The various species are distinguished primarily according to leaf shape. The varying leaf shapes led to considerable confusion among botanists in view of the fact that the leaf shape of a given species also can vary according to geographical location and even on the same plant of any species.
Antigen treatment of poison ivy is said to have been practiced by the American Indian (Gilmore, M. R., in the 33rd Annual Report, 1911-1912, Bureau of American Ethmology, Washington, D.C., Smithsonian Institution, p. 43, 1912). The methods said to have been employed by the American Indian were revived and popularized in the early part of the century (Schamberg, J. F., "Desensitization of Persons Against Ivy Poison". J.A.M.A., 73:1213, 1919). Numerous topical treatments using various chemical compounds and compositions have been proposed and used. Exemplary of such topical treatments include various oxidizing agents, for example, sodium perborate and zinc oxide. The topical treatments proposed and used over the years are intended to destroy the allergenic principle before penetrating the skin (Shelmire, B., "Sodium Perborate Ointment and Poison Ivy Dermatitis". J.A.M.A., 116(8): 681-683, 1941). Unfortunately, none of the known topically applied agents have been successful, moreover, in many cases, such agents have aggravated the dermatological condition caused by the allergens, even to the extent of spreading of initially localized erythemic and edemic reactions to other areas of the body. Reagents which are designed to act as barriers to allergens contacting the skin have also been proposed. Among such "barrier" agents are ionic exchange resins (Thurman, Francis M., Bertha Ottenstein, and Maurice J. Bessman, "Chemical and biological tests with the toxic substance of poison ivy (urushiol) and its absorption by amberlite ion exchange resins" Journal of Investigative Dermatology, 25:9-20, 1955). Unfortunately, as in the case of the variously proposed topical agents, none of the barrier chemicals have offered any degree of success. There are many known and proposed anti-pruritic agents such as calamine lotion, petrolation and steroids for use to relieve itching and inflammation. None of the known topically applied compounds or compositions have been successful in either treatment or prevention of poison ivy, poison oak, poison sumac or cashew nut shell extract caused dermatitis.
The medical profession, for many years, used treatments comprising injections of Rhus preparations (namely: ivy, oak and sumac) into humans and animals which allegedly created antibodies to the allergenic agents. Supportive evidence of the therapeutic usefulness for such treatments was based on favorable reports by clinicians in, for example,
Schamberg, J. F., "in discussion on papers of Hermann, Knowles, and White." J.A.M.A., 68:87, 1917. PA1 Schamberg, J. F., "Desensitization of persons against poison ivy." J.A.M.A., 73:1213, 1919. PA1 Schamberg, J. F., "Poison ivy treatment." Archives of Dermat. & Syph., 11:266, 1925. PA1 Alderson, H. E., "Treatment of Poison Ivy Dermatitis." California and West. Med., 23:282, 1925. PA1 Alderson, H. E. and Pruette, H. J., "Poison Oak Dermatitis (A specific treatment): Fatal results among Indians and Mexicans from eating leaves of Poison Oak plant." California State J. Med., 19:188, 1921. PA1 Bivings, F. L., "Successful desensitization and treatment of poison ivy and poison oak poisoning." Arch. Dermat. & Syph., 9:602, 1924. PA1 Williams, C. M., M.J. & Rec. (supp.), 119:131, 1924. PA1 Williams, C. M. and MacGregor, J. A., "Treatment of ivy poison by Rhus Tincture and antigen." Arch. Dermat. & Syph., 10:515, 1924.
This sanction of the use of poison ivy extracts was followed by widespread use of preparations for poison ivy hyposensitization, desensitization and treatment. Unfortunately, the clinical data supporting such treatments was found to be, for the most part, misleading and unreliable. The use of extracts created numerous problems and in quite a few reported instances dangerous pathological conditions. The medical profession now strongly denounces treatment of acute poison ivy dermatitis with such preparations. At their best, the treatment is cumbersome, time consuming, the results unpredictable, and the treatment is fraught with discomfort and danger to the patient. In the relatively few cases where desensitization has occurred, large dosage units of the toxic compound have been required over months and years and sensitivity is rapidly regained on cessation of treatment.
It is known that the dermatogenic principles contained in the resin of poison ivy, poison oak and poison sumac are a group of chemically related catechols, commonly referred to as urushiols, differing mainly in the length and degree of unsaturation of the 3-n-alkyl side chain. Poison ivy urushiol has been shown to be mainly (&gt;95%) a mixture of 3-n-pentadec-(en)-ylcatechols with 0,1,2, and 3 double bonds in the C.sub.15 side chain. Poison oak urushiol, however, consists mainly (&gt;98%) of the C.sub.17 homologues. A small percentage of the C.sub.15 congeners were found in poison oak urushiol and of the C.sub.17 homologues in poison ivy components. The analysis and identification of poison sumac urushiol is incomplete. While it has been reported that poison sumac urushiol is principally a mixture of 3-n-pentadec-(en)-ylcatechols similar to that of poison ivy, poison sumac analyzed by the inventors was shown to consist entirely of the C.sub.15 catechols with a previously undescribed principal component (&gt;60% of total urushiol) having 3 double bonds in positions different from those in the triolefinic component of poison ivy urushiol. This new component of poison sumac urushiol will hereafter be referred to as poison sumac urushiol (PSU). Cashew nut shell extract principally comprises the three compounds, anacardic acid, anacardol and cardol with varying degrees of unsaturation in the C.sub.15 side chains.
The total urushiol concentration and the relative proportion of the individual congeners may vary according to plant part, age of plant, season and place of collection. Notwithstanding, it is a well-known fact that contacting the skin of susceptible individuals or animals with any one of these plants or their constituents results in sensitization to all the allergenic compounds of the family Anacardiaceae. Heretofore, once sensitivity to any of the allergens was developed it was difficult, if not impossible, to eliminate.